提出问题：pdk1 loss of function causes a lethal phenotype in animals and yeasts, but only mild phenotypic defects in Arabidopsis thaliana (Arabidopsis).

主要结果：The Arabidopsis genome contains two PDK1-encoding genes, PDK1 and PDK2. Here, we used clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9) to generate true loss-of-function pdk1 alleles, which, when combined with pdk2 alleles, showed severe developmental defects including fused cotyledons, a short primary root, dwarf stature and defects in male fertility. We obtained evidence that PDK1 is responsible for AGC1 kinase PROTEIN KINASE ASSOCIATED WITH BRX (PAX) activation by phosphorylation during vascular development, and that the PDK1 phospholipid-binding Pleckstrin Homology domain is not required for this process.

结论：Our data indicate that PDK1 regulates polar auxin transport by activating AGC1 clade kinases, resulting in PIN phosphorylation.

Fig 7f, Only unbound PAX can be activated by PDK1S0 or PDK1, resulting in limited auxin efflux. As cellular auxin levels rise, BRX degradation and subcellular trafficking to the nucleus release PAX28, thereby facilitating activation of PAX by PDK1 and the subsequent promotion of auxin efflux by PAX-mediated PIN phosphorylation. g, In addition, auxin activates PIP5K1 expression and stimulates the concentration of PI(4,5)P2 (phospholipid in red) in the PM, resulting in enhanced PDK1 kinase activity.